“孤立淋巴濾泡”（ILFs）是小腸壁中專門的淋巴組織區(qū)域,，在那里它們參與保護宿主不受入侵病原體的侵害。對ILFs的組成及它們的形成所需因子所做的一項新的研究發(fā)現(xiàn),，它們是由來自革蘭氏陰性細菌的肽聚糖的存在被上皮細胞中的NOD1先天受體識別出而在小鼠小腸中誘導(dǎo)產(chǎn)生的,。ILFs的組成從由只有幾個B細胞構(gòu)成的細胞團到組織有序的淋巴結(jié)都有。一旦形成,，ILFs便會對細菌群落的構(gòu)成實施控制,。哺乳動物中這一由微生物誘導(dǎo)的組織形成方式的罕見事例說明，細菌與宿主之間的一種建設(shè)性互動何以能夠幫助實現(xiàn)高效消化和保護宿主不受小腸病原體侵害,。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature 456, 507-510 (27 November 2008) | doi:10.1038/nature07450
Lymphoid tissue genesis induced by commensals through NOD1 regulates intestinal homeostasis
Djahida Bouskra1, Christophe Brézillon2, Marion Bérard3, Catherine Werts4,6, Rosa Varona5, Ivo Gomperts Boneca4,6 & Gérard Eberl1
1 Institut Pasteur, Laboratory of Lymphoid Tissue Development, CNRS, URA1961,
2 Institut Pasteur, Laboratoire des Bactéries Pathogènes Entériques,
3 Institut Pasteur, Animalerie Centrale
4 Institut Pasteur, Group of Biology and Genetics of the Bacterial Cell Wall, 25 rue du Dr Roux, Paris 75724, France
5 Department of Immunology and Oncology, Centro Nacional de Biotecnologia/CSIC, UAM Campus Cantoblanco, Madrid 28049, Spain
6 INSERM, Group AVENIR, Paris 75015, France
Intestinal homeostasis is critical for efficient energy extraction from food and protection from pathogens. Its disruption can lead to an array of severe illnesses with major impacts on public health, such as inflammatory bowel disease characterized by self-destructive intestinal immunity. However, the mechanisms regulating the equilibrium between the large bacterial flora and the immune system remain unclear. Intestinal lymphoid tissues generate flora-reactive IgA-producing B cells, and include Peyer's patches and mesenteric lymph nodes, as well as numerous isolated lymphoid follicles (ILFs)1, 2. Here we show that peptidoglycan from Gram-negative bacteria is necessary and sufficient to induce the genesis of ILFs in mice through recognition by the NOD1 (nucleotide-binding oligomerization domain containing 1) innate receptor in epithelial cells, and -defensin 3- and CCL20-mediated signalling through the chemokine receptor CCR6. Maturation of ILFs into large B-cell clusters requires subsequent detection of bacteria by toll-like receptors. In the absence of ILFs, the composition of the intestinal bacterial community is profoundly altered. Our results demonstrate that intestinal bacterial commensals and the immune system communicate through an innate detection system to generate adaptive lymphoid tissues and maintain intestinal homeostasis.
